We are fat, sick and tired because of the way we live. Doctors agree in theory that a healthier lifestyle is the key to prevention. But in practice they rely on drugs. The sane solution is being serious about tackling the cause.

Guardian warns cancer diet off oncologists’ turf

All respect to the Guardian for its investigations into the murkier practices of big corporations but why does it routinely side with the heavily corporate medical mainstream when it comes to diet?

Vitamins are often dismissed as useless and possibly dangerous while recently it gave space to a piece that defined fad diets as ones that made a health claim. See more here: (See HealthInsightUK article…)

Then last month Dr. David Robert Grimes, a physicist at Oxford, laid into the very low carbohydrate “ketogenic” diet, dismissing as a ‘persistent and pernicious myth,’ the idea that it could be effective against cancer. See here: (Link). This is part of a decades-long campaign by oncologists to deny that any benefits can come from diet in the fight against cancer.

I believe that the time has come to say: ‘Enough’. Criticize the ketogenic diet – the most interesting and promising new approach to cancer for a long time – by all means but do it in an informed and thoughtful way. Don’t hand the job to a ‘postdoctoral research associate studying mathematical modelling of oxygen distribution in both vascular and avascular tumours’.

Why the ketogenic diet offers real hope

I don’t intend to insult Grimes but I believe that that he is under-qualified and over-confident for such an apparently casual dismissal. After reading the feature I asked my friend and colleague the American science journalist Travis Christofferson to write a rebuttal explaining the science behind the ketogenic diet and why it offers real hope to cancer sufferers.

Christofferson is eminently qualified to do this because he has written the definitive book about it: ‘Tripping over the Truth: The metabolic theory of cancer.’ An updated version is due to be published in the UK next month by Chelsea Green Publishing Co.

In this post – a second part will be published next week – he shows where Grimes makes a number of fundamental mistakes, such as denying that sugar from the diet feeds cancer and the claim that cancer is solely driven by genetic change.

Christofferson also explains how ketones (packets of energy the body naturally derives from fat when carbohydrate intake is very low) have a number of features that are hostile to cancer such as:

Ketones strengthens healthy cells weakens cancerous ones

‘The ketogenic diet is unique among cancer therapies in that it affects healthy cells and cancer cells very differently,’ he writes. ‘Cancer cells have difficulty using ketones and so become stressed when the body begins making them, while normal cells are actually energized by the ketogenic diet.’ As one senior researcher observes: ‘Ketones have a strange ability to make healthy cells healthier and cancer cells weaker.’

Next week Christofferson reports on what could be one of ketones most valuable contribution to treating cancer – reducing side effects. Being on the ketogenic diet for several days before and after chemotherapy has been shown to diminish ‘every one of the 14 most common chemotherapy related side-effects’.

As he says: ‘If the benefits of the diet were the myth Grimes claims, it’s odd that it is currently being investigated as a cancer therapy in over a dozen clinical trials .’

In fact the real scandal of the ketogenic diet is that bright young researchers are not becoming properly informed about it and instead write pieces that seem solely designed to prevent patients benefitting from something desperately needed by the cancer community right now – a treatments that is obviously cheap, very safe and very promising.

The real myth is that eating sugar doesn’t feed your cancer

By Travis Christofferson

Before I go into why Grimes’ attack is based on several serious misunderstandings, I need to answer the most basic question: What is the ketogenic diet? Here comes a quick biochemistry lesson. Your body, like a hybrid car, can burn two types of fuel. It’s been designed that way by millions of years of evolution.

The fuel we all know about is sugar/glucose which comes from carbohydrates. The other much less familiar type is known as ketones – small energy dense molecules which the body makes in the liver from fat. It’s a kind of back-up system that automatically kicks in when carbohydrate/glucose supplies run low. So a ketogenic diet involves eating almost no carbohydrates and replacing them with fat.

And what has this got to do with cancer? Healthy cells can make energy in small ‘power plants’ called mitochondria using either glucose or ketones. Some athletes claim that ketones are a better source of fuel for long distances. Crucially the mitochondria in cancer cells don’t work very well, if at all, so the cells have to switch to a cruder and less efficient system called glycolysis which needs much larger glucose supplies than the mitochondria route.

Simple: remove cancer’s preferred source of fuel

Going ketogenic can damage cancer cells because not only are they getting less glucose in the blood but their faulty mitochondria can’t use ketones. So the logic behind the ketogenic diet as a cancer therapy is seductively intuitive: remove the cancer cells preferred source of fuel and replace it with a fuel it has difficulty burning. Simple

Given this very plausible scenario it’s probably a big mistake to categorically claim the ketogenic diets is a “cancer treatment myth.” Especially if your life is at stake. Grimes attempts to challenge the scenario by saying changing diet is flawed from the very git-go because cancer is caused by mutations to DNA—and therefore any dietary intervention “can’t affect cancerous cells.” The dogmatic assumption that cancer is exclusively a genetic disease, however, is a position that’s becoming harder and harder to maintain.

A massive governmental effort to understand the genetic underpinning of cancer, called The Cancer Genome Atlas (TCGA) project that kicked off in 2006 (and concluded in January of 2015) has left many cancer researchers scratching their heads. Its findings have shaken the very foundation of the standard theory of cancer.

Cancer not exclusively caused by DNA mutations

This is the one we all know about, which says that cancer is the result of a relatively small number of ’driving’ mutations turning a healthy cell cancerous and causing it to grow uncontrollably. This would allow them to be targeted with drugs. However, this is not what the atlas shows; the most defining feature of the cancer cell genome as revealed by TCGA is that it is completely chaotic.

The TCGA sequenced the entire genomes from 10,000 malignant tissue samples and reportedly discovered 10,000,000 cancer related mutations but there was no clear pattern. Some cancers had 20 or more mutations; others might have just one mutation or even none at all. The conclusion: cancer is not exclusively caused by mutations to DNA. It can’t be. Something else must be causing and driving it.

TCGA was intended to be our last battle with cancer, we would finally know it in it’s entirely, but rather, it left us with a murky, muddled mess. A 2015 Nature article titled End of cancer-genome project prompts rethink, highlighted the confusion:

A bewildering hodgepodge of genetic oddities

“Also a problem was the complexity of the data. Although a few ‘drivers’ (driver are genes that when mutated cause or ‘drive’ cancer) stood out as likely contributors to the development of cancer, most of the mutations formed a bewildering hodgepodge of genetic oddities, with little commonality between tumors.”

This is what James Watson, the Nobel Prize winning co-discover of the structure of DNA, said of TCGA:

“We can carry on and sequence every piece of DNA that ever existed, but I don’t think we will find any Achilles heels. We’ve had about 10 years. It’s not the story I wanted to hear. I would have hoped for a lot more success.”

If mutations to DNA are not the entire picture, as Grimes claims in his article, then what is the ultimate cause of cancer? We’re still trying to figure that out.

Cause of cancer; more than one way to skin a cat

What we do know, is that something called epigenetics—the turning on and off of genes—is involved in transforming a normal cell into a cancerous one. Dr. Jean Pierre Issa of M.D. Anderson, a tremendously respected cancer researcher, said in an interview for NOVA, a division of Public Broadcasting:

“Up until recently the idea was that cancer is a disease of genetic changes. The genes themselves, their structures, become abnormal. Over the past few years we have come to realize that there might be more than one way to skin the cat—that there might be changes other than genetic changes that would account for the bizarre behavior of cancer cells. And these relate to epigenetics.’

Epigenetic changes—the turning on and off of genes without changing the underling sequence of DNA—are responsible for a striking metabolic shift within the cancer cell. This involves a major change in the way cancer cells make energy.

This dates back to 1924 the great German biochemist Otto Warburg discovered that cancer cells were doing something strange. Unlike normal cells they were making most of their energy via a method called ‘aerobic fermentation’. Also known as glycolysis. It involves burning glucose (sugar) very fast and making lactic acid in the process. Today this metabolic quirk of the cancer cell is called the Warburg effect.

Cell turns into a sugar consuming machine

Normal cells make 90 percent of their energy in the tiny power plants found in almost every cell in the body called mitochondria. They use oxygen and don’t produce lactic acid. We now know how cancer cells switch to the Warburg effect but the reason why is still hotly debated.

They do it by changing the amount of protein produced by a gene called hexokinase 2. The gene doesn’t change it just becomes more active – this is epigenetics. The result is the cell turns into a sugar consuming machine.

So Grimes got something else very important wrong when he wrote: “In 1924, Otto Warburg suggested this metabolic switch to glycolysis might drive cancer. Subsequent investigations showed that in fact the switch actually stems from the very mutations that give rise to cancer – basically, it’s a consequence of cancer rather than the cause.”

I’ll give Grimes 1000 dollars—to donate to his favorite charity—if he can show me a single mutation that is a cause of the Warburg effect—not just a trigger of the epigenetic shift to hexokinase II.

Grimes claim on sugar absolutely wrong

The reason why it matters whether the energy production switch is due to a mutation or to epigenetics is because an epigenetic change can be reversed, unlike a mutation.

If you’ve seen a PET scan, you’ve seen a visual image of the Warburg effect. A PET scan is done by injecting radiolabeled glucose into the patient. The “hot spots” that then appear are a dramatic visualization of cancer voracious appetite for sugar.

This too is absolutely wrong. This is the basis of a PET scan. Without the ability of sugar to “gravitate” and become concentrated inside cancer cells, the PET scan would not exist. In fact there is no argument about cancer’s love of sugar which leaves the basic idea behind the ketogenic diet – energy reduction – untouched.

Next week:The experts who are investigating the ketogenic diet and the growing evidence that it can dramatically reduce the damaging side effects of chemotherapy while improving outcomes. Also how the bar for gathering evidence to show that non-drug treatments are safe and beneficial is set far too high and damages patients.

Travis Christofferson

Travis Christofferson is a science writer and a graduate of the Montana State Honors Program in molecular biology. He also has an M.S. in Material Engineering and Science from the South Dakota School of Mines and Technology. He is the author of the bestselling book 'Tripping Over the Truth: The Metabolic Theory of Cancer'. It gives an historical perspective on the re-emerging theory that cancer is triggered and driven by damage to mitochondria.
Link

However, this is the sort of evidence that strengthens the case for a medical theory, because it has to be specific to be credible. Cancers are a variety of very different conditions, and to claim that any treatment will have the same effect in every case is inherently implausible.

For example, it can clearly be demonstrated that the ketogenic diet works in regard to inhibiting prostate cancer in the study I cited, and in the melanoma study has no effect on one type of melanoma (leaving open the possibility that a better-designed ketogenic diet might), and a growth promoting effect on the other.
These are different tumour cells with different natural histories, and it seems obvious that some rely on glycolysis, some may be inhibited by ketones, and some prefer ketones, or perhaps specific ketogenic fatty acids.

What makes the ketogenic diet so interesting and promising is that the majority of cancers do change the way they generate energy which suggests a range of new targets that might well be found in a variety of cancers. Prostate cancer may well be one where it is not effective but there is promising research to show it can benefit brain cancer – one that is particularly hard to treat otherwise.

It’s worth remembering, when swapping studies supporting either side, that there is a vast imbalance in resources. The number of researchers trying to unravel the intricacies of ketones and cancer across the board is tiny compared with the number of well funded scientists working on the next generation of a single biologic for a single cancer.

The real question is not, Why has this or that aspect of the ketogenic theory not been sorted out but why are cancer charities, funded by us to “beat” cancer, not doing any research into it at all? Instead they seem content to continue recommending the low fat ‘healthy balanced diet’.

Yes, it seems to be effective for prostate cancer (though I would limit linoleic acid because there is evidence that consumption of this fatty acid is increased by PC cells and used to make prostaglandins which promote growth), seems to harmful for one type of malignant melanoma, and is at worst neutral for another. Neurogliomas I think there is good evidence for efficacy, and I’d predict this for leukaemia too based on its metabolism.
But all of these cancers have, like the melanomas, genetically diverse types, some of which may tolerate ketosis better than others.
I think this is unlikely for brain cancers and cancers in cells that normally have high glucose use such as immune cells.
If fat promoted cancer globally then cancers of adipose tissue would be the most common cancers, which of course they are not.

Thanks for pointing out that prostate is actually one that benefits from ketones, misread Henderson’s post. But there are some that don’t- which they are is just one of many questions that a patient focused research program would be sorting out. Ignoring patient feedack is one of the signs of an area where the mainstream is getting it wrong. Think addiction and suicide potential of SSRI antidepressants and statin side-effects.

Hi Stephen – have a look at Yes to Life – a small UK charity which actually supports people with cancer who look at taking an integrative approach. If you fancy contributing to a cancer charity – you really should seek one that aims to support people’s choice

Great points George. More research will be needed to,untangle which cancers the ketogenic diet works best for. Theoretically, any cancer that is PET positive should be affected. Some very interesting research is being done on the epigenetics of ketones. BHB’s histone deactylace inhibitory activity is shown to turn down about a dozen cancer related genes; HIF 1 alpha, TNF, VEGF, ect.. It’s important to note that a histone deactylace inhibitor is already approved for a type of leukemia and is in over 80 trials. The problem is BHB is free, so ironically, it will never get the backing for a clinical trial.

The Ketogenic diet does work. It works A WHOLE LOT BETTER when Coconut oil and coconut is used as a ready source of ketones as well as the Adaptogen it is… in bringing about body systems functions cancers disrupt, as well as being the antibacterial, antiviral, antifungal, and antiprotezoal that it is too. Drop not only the sugars and carbs, but most PUFA oils too. USE Coconut oil, Red Palm oil, Olive oil, Butter, Avocados, fresh nuts and seeds. I was losing my battle until I made these switches. They were far enough spaced (discovery without guidance was slow) that I could make direct observation on improvements. Healing up damage can be as important as arresting and starving out the cancer. It was a couple of years literally later that I stumbled across Travis Christofferson’s book Tripping Over the Truth and Dr. Thomas Seyfried’s Cancer As A Metabolic Disease. Read Dr Bruce Fife’s The Coconut Oil Miracle and his book The Palm Oil Miracle. It works. People need to know this now.

Very many years ago, I remember reading about some research testing two very simple compounds, dimthylsulphoxide (DMSO), and something else whose name I forget, as ‘miracle’ cancer cures.

On reading above that some tumour cells were found to have no mutations at all, I remembered that article because the theory was that these two compounds were able to convert cancer cells back into ordinary cells. Of course, if cancer was caused by a mutation, this seemed very unlikely.

A quick GOOGLE found this article – still using DMSO, but with a different proposed mechanism of action:

Thanks for a really interesting conversation. A question to all of you that has had me pondering for a long while. I am a cancer thriver, managing metastasised prostate cancer. I am on an extreme vegan diet, in the belief that I need to keep IGF-1 levels low (in addition to low glucose). I am very interested in the ketogenic diet but my vegan proteins come coupled with carbs (eg grains, lentils, pulses). So it seems that veganism and ketogenic are competing theories. I would love to hear your views. Thanks in anticipation.

Hi Nick,
my understanding is that a vegan diet, if you do it right, is full of phytochemicals that can be more-or-less toxic to some cancer cells (though the science of this with regard to humans is a bit hit-or-miss, is seems plausible enough). Because it is low fat and protein it will, if you were non-diabetic to start with, keep insulin and IGF-1 levels low. And being low fat you won’t have much omega-6 linoleic acid in LDL particles, which is what prostate cancer seems to thrive on.

Hi Nick, I’ve heard of people doing vegan versions of the keto diet although it is more difficult. I think one of the reasons the keto diet works for cancer is because it drastically lower IGF-1. When calculating macro ratios remember carbs and protien are bundled together on the keto diet because both raise blood sugar (and IGF1).

Well hello Mathew I do admire your persistence. I remember our exchange here some months ago over low carb diet in reference to a post headlined “Clash of Titans”. I also remember being irritated at your habit of firing off references that didn’t actually come to the conclusion you claimed and then when this is pointed out ignoring the rebuttals and swiftly posting some more claims. Made responding time-wasting and frustrating.

Sorry to find – after time-wasting checking of your references – that little has changed.
But before dealing with references I have to politely ask you not to behave like a troll – even if you are one – and include superfluous insults and allegations in your comments. “To enncourage a ketogenic diet is to increase your risk of death and disease Travis”.

First point on all the references is that they relate to observational studies and so cannot prove causation. Secondly several rely on the notoriously unreliable food questionnaires. In one, for example, “women recorded their frequency and quantities of consumption of about 80 food items and beverages, focusing on the six month period before their enrolment in the study”. Who reliably knows how much broccoli or peanut butter they ate in the last six months?

This was study 2 which looked at a high protein/low carb diet (the definition of ‘high’ is not clear) in woman aged 40 to 50 (so not relevant to men or older people such as those most likely to have cancer). It came to the surprising conclusion that “a 20 g decrease
in daily carbohydrate intake and a 5 g increase in daily protein intake would correspond to a 5% increase in the overall risk of cardiovascular disease.”

I’ll leave it someone else to do the detailed maths but since 200 gms of carbs is not uncommon in a standard diet and a low carb diet could go down to 20gms that is getting on for a 50% increase in heart disease if you go on a low carb diet for 20 years or so. None of these studies showed anything like that.

So your allegation that low carb diets are killing people looks pretty shaky. But then the conclusion of this study provides no basis for your claim at all. The authors write: “Our results do not answer questions concerning possible beneficial short term effects of low carbohydrate or high protein diets in the control of body weight or insulin resistance.” The diet that Travis is promoting is intended to be used in the short to medium term to help cancer patients with glucose levels which are related to insulin levels.

The third reference makes the situation even more murky. This one says that is a higher risk of all cause mortality but not of heart disease – precisely the condition the other studies claimed to find an association with. It then calls for more trials to sort out the issue. Again no support for the ‘you are killing people’ allegation.

This is the conclusion: “Low-carbohydrate diets were associated with a significantly higher risk of all-cause mortality and they were not significantly associated with a risk of CVD mortality and incidence. However, this analysis is based on limited observational
studies and large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes are needed”

And finally the 4th reference from the Harvard group that has been supporting low fat for a long time. It did find an association (note not cause) between risk of all cause mortality and low carbs but this was on a group of patients who had had a heart attack and so not directly relevant to the cancer patients Travis to talking about.

Finally I am really puzzled by your attitude. The ketogenic diet looks like it has the potential to revolutionise the treatment of not only cancer but also diabetes. It opens up all sorts of avenues to prevent and treat these conditions that are claiming lives in numbers that are reaching epidemic levels. Isn’t a sane and scientifically literate response: How remarkable lets find out more”? Instead you feel it is relevant to dig up four obscure trials that raise the issue of a long term risk of mortality from the diet.

Even if it did turn out there was a raised risk of dying earlier (how many days or months might that be?) from the diet decades in the future, how on earth is that relevant to someone using the diet to make chemotherapy more effective and cut the level of side effects in treatment of a cancer that may kill them in a matter of months?

Sorry Matthew that’s it. I went into detail in reponse today in case the claim that the ketogenic diet kills people got any traction but I’m not engaging with your comments in future as i consider it a waste of time and if you do comment again I will trash it if I feel it is not contributing to the debate in a useful or informed way.

“Matthew”, should be found and disabled. Advocating people to consume high carbs. Exclusively sourced from vegetables, i.e broccoli is the goal, not refined sugar garbage. Once a week, these carbs are bumped up a notch, whilst during the week, they are very low. This negates the rubbish that doctor you used, spouts.

Don’t really agree with ‘disabling’as we do welcome discussion here but making claims backed by irrelevant references is not a useful contribution. Also i wonder why he needs to shelter behind a pseudonym. Perhaps these days ‘fakename’ would be a more appropriate term.

It is my real name. Why would I need a fictitious name here Mr Ed. You stil haven’t answered whether you would be so confident to reply direct to Mcdougall via his open youtube webinar. Tomorrow, Thursday 7:00pm.

Despite Matthews objections to the ketogenic diet it is highly probable that he followed one once.

Mothers milk is rich in fat and so suckling infants (of any species of mammal) rely heavily upon the intermediary metabolites of fats (ketone bodies) to fuel cells, cell proliferation, and growth.

Formula milk ought to be a decent imitation of the nature and constituents of breast milk – if it isn’t that would be a crime against nature – and so irrespective of the mothers choice to breast feed or formula feed baby the balance is essentially keto.

Matthew must have been a baby once. He seems to think that he is all grown up now but what I read between the lines of his comments assures me of a significant degree of immaturity. It reminds me of playground disputes and exchanges along the lines: “My brother is bigger than your brother”.

Matthew coveys an attitude that is a little bit more grown up but not much: “My guru knows better than your guru. Nah-ne nah-ne nah nah”

Worse, at times his style of writing is just plain aggressive.

I wonder if what Dr. Hibbeln of the NIH has to say about omega-6 PUFAs can cast light.

Increases in world consumption of omega-6 PUFAs may have increased the societal burdens of aggression, depression, and cardiovascular mortality, his words have directed.

Experimentation involving making extra omega-3 fats available to prisoners diminished incidences of aggression and aggressive acts. Part of the problem with omega-6 fats is that they are physiologically competitive with omega-3 types. Over-consumption of omega-6 fats negate the benefits normally attributable to the omega-3 types.

I steer as clear as I can away from margarines and veg oils. Feel much better, much less depression, fewer aggressive thoughts, and haven’t been in a scrap since I made the changes. Perhaps Matthew is a nice guy really but one whose attitudes have been negatively impacted by overdosing on the margarine and veg oil.

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Matthew might like to take up interest with the work of Cynthia Kenyon. Ms Kenyon studies model organisms for what they have to say about metabolism and ageing. Her model organism of choice is caenorhabditis elegans (C. elegans, for short).

C. elegans is a tiny nematode (round worm) not much more than 2mm long. Amongst its attractions for researchers is that it is reasonably translucent; so with the aid of a microscope developmental biology researchers can peer inside and observe what is going on.

Sometime back in the 1980s a study reported that placing mice upon a calorie restricted diet could extend their life. Other similar studies have reported similar results and arising in other species. This study gained traction in popular media and so people learned of it that other wise might not.

The claims for longevity and calorie restriction sat well with the prevalent and easily accepted calorie hypothesis for obesity and the overweight. And since fats are so dense in calories the bandwagon the experts jumped on everybody touted that the way to lose weight is to consume less fat. It is an odd thing; that people have become so much more overweight in the time that the calorie hypothesis for obesity has prevailed.

Debates have raged over the mechanism of how calorie restriction actually works. Was it calorie restriction?, was it reductions in degrees of adiposity?, was it a reduction of oxidative stress?, or was connected to hormones?

It became clear to Ms Kenyon that the genetic mutations in C. elegans that promoted longevity were the ones that diminished the activity in the worms insulin / insulin-like growth factor (IGF) pathway. She then wondered what would happenis she fed worms some glucose in addition to their normal diet of bacteria. Just 2% addition of glucose to the bacterial medium diminished life-expectancy of her worms by a full quarter.

Her hypothesis amounts to a reversal of the implications from the genetic modifications. If genetic remapping and reductions in insulin / IGF activity prolong life expectancy glucose shortens it by increasing activity within that same pathway. The day she realised glucose shortened the life of her worms she elected to restrict her own consumption of carbohydrates. She does not exclude them but she is devoted to excluding those with a high-glycemic-index. She lost thirty pounds and all those metrics included in medical work-ups improved. Blood pressure normalised, triglycerides and blood sugar fell, while her HDL increased.

That excess weight is accompanied by by an elevated risk of chronic is a given. The questionable assumption is to wonder if counting calories actually does any good. The old and familiar calorie hypothesis suggests that it should. Patterns of rising incidence witnessed in recent decades suggests that it isn’t. The alternative assessment might be that obesity is driven by hyperinsulinemia which in turn is driven by the low fat high carbohydrate diets that all that healthy eating advice has encouraged people to follow.

Again patterns of incidence involving obesity, diabetes, complications from diabetes, heart disease, cancer, and dementia are all strikingly similar. They arise more frequently amongst certain peoples living life in certain places and eating certain diets than they do in others. And in the places where incidence is greatest incidence has been on the rise and continues to rise. Furthermore peoples who once lived outside of western dietary influences (the Inuit, say, or Australian Aboriginals) that turn their back on old lifestyles to adopt more ‘westernised ways’ with all the appeal of fast food and sodas very quickly trend from being healthy to alarming incidence of chronic disease.

The debates are still raging and they do so because the medical fraternity are a conservative lot resistant to new ideas that refuse to concede the folly in old hypotheses. The insulin / IGF hypothesis for ageing, degeneration, and chronic disease hasn’t addressed all the questions it invites and it hasn’t resolved all former arguments, but it is gaining traction.

“If you tell people to follow a Low-Carb Diet you sicken and kill people.”

Astonishing in the light of how the health of people in developed nations has been in steady decline and the extent to which people have been medicalised by being dependent tablets for this, that, and the other. Any person who is over fifty and not taking one or more prescription medicines is becoming a rarity. How can that be deemed a success? It can’t and the costs are bringing health services to their knees.

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The lessons from mammals ranging wild and free in nature is that gaining condition (body fat) in the months of plenty is great life insurance for when food is scarce in the months of privation. The grisly bear spends six months of the year and thus survives winter by burning ketones from body fat that was accumulated during summer. Then when he wakes up he is driven by rising cortisolemia and insulinemia to feed like crazy and thus restore condition for another winter.

The bears metabolsim has circadian swings between the anabolism of summer and the catabolism of winter. The grisly is represents an instance of extreme physiology but the principles at work are universal amongst mammals.

So if a human ate just one balanced meal a day how is ingestion of fuel (in a single lump sum) to be reconciled against an energy requirement that is relatively constant over 24 hours? The answer is the the bodies metabolism must be able to buffer energy in some way. That essentially is an affair of storage and recall arising within 24 hours. I suspect that in this instance metabolism will be making adjustments along the lines of shifting emphasis between anabolism (burning glucose) and catabolism (burning ketone bodies). In other words circadian shifts in emphasis are a natural requirement of coping with meals and the time between meals.

The stark reality is that so many people are overweight if not actually clinically obese. If swings in metabolic emphasis could be deemed normal and part of the circadian balance then the overweight and obese have not got the balance right and have spent too much time driving anabolism and not enough time creating opportunities for catabolism.

So much rests upon perturbation of of insulin levels. And whilst they are not the only influence to perturb insulin they probably deserve to be ranked the highest.

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“Matthew, your confusing what you believe (others do not) is the optimal diet for longevity with a medical intervention for a potentially terminal illness.”

Great comment very wide ranging, putting the debate in not just an evolutionary but in a web-of-life context. Does show how far medics and dietitians for that matter have strayed from basic understanding of how our bodes work when a natural process – producing ketones – is seen as deadly. It is an approved treatment for childhood epilepsy for heaven’s sake

There are some news about the subject.
Follows the abstract of an article published this month that offers an alternative hypothesis advocating stress, by inducing lactate production, as the primary cause of cancer:
- Carlos ETB Monteiro, “Stress as the Inductive Factor for Increased Lactate Production: The Evolutionary Path to Carcinogenesis”. Positive Health Online, Edition 241, October, 2017 at http://www.positivehealth.com/article/cancer/stress-inductive-factor-for-increased-lactate-production-evolutionary-path-to-carcinogenesis
Abstract
In the present paper is discussed about the recent evolution in the understanding of the role of lactate formation in promoting cancer.
On it is postulated the hypothesis that chronic stress is the major risk factor and inductor of the increased lactate production which might lead to the carcinogenic process. It also explains how stress develops lactate formation, what was discovered in 1925.
The current hypothesis support ketogenic diets for prevention and therapy for cancer. This inside the reasoning that while fats do not have appreciable effects on the sympathetic nervous system (SNS) or in lactate formation, high carbohydrate diets have significantly effects on both SNS and lactate formation.
At the end of the paper has a short explanation and link to a parallel article where is discussed cardiac glycosides (ex.: digitalis like digoxin) as the fundamental drugs for prevention and treatment of cancer.

BTW, in a study published in October 6, 2017, the researchers showed lactate is not only a waste product but also acts as a fuel source consumed by lung cancer cells growing in patients and mice. The full free text is at http://www.cell.com/cell/pdf/S0092-8674(17)31068-1.pdf

The link is to an article about the guy who wrote an article (one among many others) in the Guardian several months ago explaining why the idea that the ketogenic diet could not have any effect on cancer was a myth. Grimes’ article was comprehensively debunked here on HIUK by Travis Christofferson who wrote an excellent book on the the origin’s of the idea that reducing sugar and insulin and so cutting cancer’s energy supply made a lot of sense.

This link looks at the faulty scientific logic behind Grimes’ rejection of environmental causes of cancer and his steadfast defence of the random mutations theory which has serious logical and empirical flaws which Christofferson dissects in his book